Hemodynamic Factors May Play a Critical Role in Neurological Deterioration Occurring within 72 hrs after Lacunar Stroke

et al. (2014) Hemodynamic Factors May Play a Critical Role in Neurological Deterioration Occurring within 72 hrs after Lacunar Stroke. PLoS ONE 9(10): e108395. doi:10.1371/journal.pone.0108395 Hemodynamic Factors May Play a Critical Role in Neurological Deterioration Occurring within 72 hrs after Lacunar Stroke Yen-Chu Huang 0 Yuan-Hsiung Tsai 0 Jiann-Der Lee 0 Hsu-Huei Weng 0 Leng-Chieh Lin 0 Ya-Hui Lin 0 Chih-Ying Wu 0 Ying-Chih Huang 0 Huan-Lin Hsu 0 Meng Lee 0 Hsin-Ta Yang 0 Chia-Yu Hsu 0 Yi-Ting Pan 0 Jen-Tsung Yang 0 Marle`ne Wiart, Creatis UMR CNRS 5220, France 0 1 Department of Neurology, Chang Gung Memorial Hospital at Chiayi, Chang-Gung University College of Medicine, Chiayi, Taiwan, 2 Department of Diagnostic Radiology, Chang Gung Memorial Hospital at Chiayi, Chang-Gung University College of Medicine, Chiayi,Taiwan, 3 Department of Neurosurgery, Chang Gung Memorial Hospital at Chiayi, Chang-Gung University College of Medicine, Chiayi, Taiwan, 4 Department of Emergency Medicine, Chang Gung Memorial Hospital at Chiayi, Chang-Gung University College of Medicine , Chiayi , Taiwan Background: Whether a perfusion defect exists in lacunar infarct and whether it is related to early neurological deterioration (END) is still under debate. The aim of this study was to evaluate whether END in lacunar infarct is related to a perfusion defect using diffusion-weighted imaging (DWI), diffusion tensor imaging (DTI) and perfusion MR imaging. Methods: One hundred and forty-one consecutive patients had an MRI scan within 30 hours after onset of symptoms and 43 patients with acute lacunar infarct and classic lacunar syndrome were recruited. The MRI sequences included DWI, DTI and cerebral blood flow (CBF) maps to respectively represent the topographic locations of acute infarcts, the corticospinal tract and perfusion defects. The END was defined in reference to the National Institute of Health Stroke Scale (NIHSS) as an increase 2 within 72 hours. Cohen's Kappa coefficient was used to examine the reliability between the 2 image readers. A multivariate logistic regression model was constructed adjusting for baseline variables. Results: Ten out of the 43 patients had END. Patients having END was significantly associated with lower chances of favorable and good outcomes at 3 months (p = 0.01 and p = 0.002, respectively). END was predicted when the non-core hypoperfused area overlapped on the corticospinal tract, which is defined as the expected END profile. Cohen's Kappa coefficient between the 2 image readers to define images of expected END profiles was 0.74. In 15 patients with expected END profile, 9 had END clinically, whereas 28 patients had no expected END profile, and only 1 patient had END (p,0.0001). After adjusting for sex, the expected END profile was still associated with END (odds ratio, 42.2; p = 0.002). Conclusion: Our study demonstrated that the END in acute lacunar stroke is likely related to the transformation of non-core hypoperfused area into infarction in the anatomy of corticospinal tracts. - Funding: This work was supported by Chang Gung Memorial Hospital grants CMRPG690451, CMRPG690452 and CORPG690453. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing Interests: The authors have declared that no competing interests exist. Background and Purpose Early neurological deterioration (END) in acute stroke often leads to poor functional outcome. Progressive motor deficits are the main manifestations of END in lacunar lacunar infarct [1]. However, there may be different pathologies underlying lacunar infarcts: atherosclerosis or embolism affects larger perforating arterioles while lipohyalinosis affects smaller arterioles [2]. Lacunar stroke caused by atheromatous occlusion at the orifice of large caliber penetrating arteries, termed branch atheromatous disease, is associated with the higher possibility of progressive motor deficit compared to that by lipohyalinosis [3]. The pathophysiology of progression is still incompletely understood and may be related to a hemodynamic defect, extension of thrombosis, excitotoxicity, or inflammation [4]. Although perfusion abnormalities are likely to play a critical role in END in acute stroke [5], there is still uncertainty whether a penumbra exists in lacunar infarct and whether END is related to perfusion deficit. Gerraty et al. observed in a perfusion MRI study that a perfusion defect only existed in striatocapsular artery infarction due to large artery atherosclerosis or embolism but not in lacunar infarcts [6]. However, Yamada et al in a perfusion CT study used cerebral blood flow (CBF), cerebral blood volume, and mean transit time (MTT) to predict the progression of lacunar infarct in the territory of the lenticulostriate artery within 24 hours of onset. Their results showed that lower CBF and higher MTT were related to END, and they hypothesized that hemodynamic insufficiency is related to the progresses of infarction [7]. In another study, perfusion abnormalities (decreased CBF and delayed MTT) were found in two thirds of patients with lacunar infarcts, and those with normal perfusion image were free of deterioration. However, abnormal perfusion image was not significantly related to END [8]. The discrepancy between these studies may be partly due to the small infarct size of lacunar infarct, and the enlarged infarct area may not exactly lead to progressive motor deficit if the corticospinal tract is not involved. This is why END in lacunar infarct has been found to be highly related to the relationship between the location of infarct and corticospinal tract [9,10]. Alawneh el al. found that the non-symptomatic area in oligemia, which is called non-corenon-penumbral tissue, carried a higher risk of infarct and was associated with the worsening of early neurological deficits [11]. The hypothesis of this study is that END in lacunar infarct is related to the transformation of a perfusion defect into infarction in the area of the corticospinal tract. To confirm this hypothesis, we used diffusion-weighted imaging (DWI) and MR perfusion imaging to define the infarct lesion and perfusion defect, termed non-core hypoperfused area, of each patient. The corticospinal tract was defined by diffusion tensor imaging (DTI), which has been applied with good correlation to trace the corticospinal tract to both clinical motor deficits and the prognosis in patients with lacunar stroke [12,13]. Patients This prospective study was conducted from December 2010 to December 2013 and was part of an integrated stroke project at Chang Gung Memorial Hospital. In the integrated stroke project, patients with suspected stroke were selected and underwent MRI Stroke onset to MRI (hr) Favorable outcome at 3 months Good outcome at 3 months within 30 hours after the onset of symptoms. Patients with contraindications to MRI study or gadolinium injection were (...truncated)